Centre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 3EG, UK.
Centre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 3EG, UK.
Placenta. 2020 Sep 15;99:131-140. doi: 10.1016/j.placenta.2020.07.010. Epub 2020 Jul 22.
The placenta performs a range of functions to support fetal growth. In addition to facilitating nutrient transport, the placenta also stores glucose as glycogen, which is thought to maintain fetal glucose supply during late gestation. However, evidence to support such a role is currently lacking. Similarly, our understanding of the dynamics of placental glycogen metabolism in normal mouse pregnancy is limited.
We quantified the placental glycogen content of wild type C57BL/6JOlaHsd mouse placentas from mid (E12.5) to late (E18.5) gestation, alongside characterising the temporal expression pattern of genes encoding glycogenesis and glycogenolysis pathway enzymes. To assess the potential of the placenta to produce glucose, we investigated the spatiotemporal expression of glucose 6-phosphatase by qPCR and in situ hybridisation. Separate analyses were undertaken for placentas of male and female conceptuses to account for potential sexual dimorphism.
Placental glycogen stores peak at E15.5, having increased over 5-fold from E12.5, before declining by a similar extent by E18.5. Glycogen stores were 17% higher in male placentas than in females at E15.5. Expression of glycogen branching enzyme (Gbe1) was reduced ~40% towards term. Expression of the glucose 6-phosphatase isoform G6pc3 was enriched in glycogen trophoblast cells and increased towards term.
Reduced expression of Gbe1 suggests a decline in glycogen branching towards term. Expression of G6pc3 by glycogen trophoblasts is consistent with an ability to produce and release glucose from glycogen stores. However, the ultimate destination of the glucose generated from placental glycogen remains to be elucidated.
胎盘具有多种功能，以支持胎儿生长。除了促进营养物质的运输外，胎盘还将葡萄糖储存为糖原，这被认为可以维持胎儿在妊娠晚期的葡萄糖供应。然而，目前缺乏支持这种作用的证据。同样，我们对正常小鼠妊娠中胎盘糖原代谢动力学的理解也很有限。
我们定量分析了野生型 C57BL/6JOlaHsd 小鼠胎盘的糖原含量，从中期（E12.5）到晚期（E18.5）妊娠，并对编码糖生成和糖原分解途径酶的基因的时空表达模式进行了特征描述。为了评估胎盘产生葡萄糖的潜力，我们通过 qPCR 和原位杂交研究了葡萄糖 6-磷酸酶的时空表达。分别对雄性和雌性胚胎的胎盘进行了分析，以解释潜在的性别二态性。
胎盘糖原储备在 E15.5 时达到峰值，比 E12.5 时增加了 5 倍以上，然后在 E18.5 时又减少了同样的程度。E15.5 时，雄性胎盘的糖原储备比雌性高 17%。糖原分支酶（Gbe1）的表达在接近足月时降低了约 40%。葡萄糖 6-磷酸酶同工型 G6pc3 的表达在糖原滋养层细胞中富集，并在接近足月时增加。
Gbe1 的表达减少表明糖原分支在接近足月时减少。糖原滋养层细胞表达 G6pc3 表明它们有能力从糖原储备中产生和释放葡萄糖。然而，胎盘糖原产生的葡萄糖的最终去向仍有待阐明。
